An organism's ability to detect and respond to environmental stimuli is critical for its survival. It is particularly important for animals to incorporate contextual information, such as internal state or external cues, in order to modify behavioral responses and maximize fitness. This behavioral plasticity has largely been studied in the context of learning or adaptation. However, how environmental cues modulate the valence of innate responses to nave stimuli remains poorly understood. Behavioral plasticity can stem from genetic, molecular, and circuit level changes in neural function, ultimately leading to an organism's ability to thrive in a dynamic environment. The overall goal of my thesis is to investigate the molecular and neuronal mechanisms underlying olfactory plasticity in C. elegans. Preliminarily, I have found that while C. elegans grown under sparse culture conditions avoid high concentrations of the volatile chemical 1-hexanol, animals grown at high population density are instead robustly attracted to this odorant. My results indicate that this plasticity in olfactoy responses is mediated by pheromones, which may serve as a population density cue. I will exploit the experimental amenability of C. elegans to identify the genes, neurons and circuits that underlie the responses to 1-hexanol, and investigate how these responses are modified by contextual cues and experience. To do so, I will utilize a novel quantitative approach and high-resolution data analysis algorithms. Insights from this research will shed light on conserved molecular and neuronal pathways involved in sensory plasticity. Many neurological disorders-from developmental disorders such as autism to neurodegenerative diseases such as Alzheimer's and Parkinson's-stem from underlying deficits in neuroplasticity. Therefore, in addition to understanding the mechanisms of plasticity in a healthy context, this work has important implications for understanding the mechanisms underlying disease states.